This chapter comprehensively reviews a new and emerging body of scientific evidence related to the use of e-cigarettes by youth and young adults. The enormous knowledge base on tobacco smoking and human health is also relevant to this discussion. That literature, which has been accumulating for more than 50 years, provides incontrovertible evidence that smoking is a cause of dis-ease in almost every organ of the body (U.S. Department of Health and Human Services [USDHHS] 2004, 2014).
Laboratory research has characterized the components of tobacco smoke and probed the mechanisms by which these constituents cause addiction and injury to cells, tis-sues, organs, and the developing fetus.
The evidence on the harmful consequences of nic-otine exposure in conventional cigarettes, including addiction, and other adverse effects, is particularly rel-evant to e-cigarettes. Nicotine doses from e-cigarettes vary tremendously depending on characteristics of the user (experience with smoking conventional cigarettes or e-cigarettes), technical aspects of the e-cigarette, and levels of nicotine in the e-liquid. Although studies of nico-tine doses in youth and young adults are lacking, studies of adults have found delivery of nicotine from e-cigarettes in doses ranging from negligible to as large as (Lopez et al. 2016; Vansickel and Eissenberg 2013; Spindle et al.
2015; St. Helen et al. 2016) or larger than (Ramôa et al.
2016) conventional cigarettes. Similarly, passive exposure to secondhand nicotine from e-cigarettes is just as large
(Flouris et al. 2013) or lower than (Czogala et al. 2014) conventional cigarettes.
The findings of scientific research on smoking and involuntary exposure to tobacco smoke have been reviewed thoroughly in the 32 reports on smoking and health produced by the Surgeon General to date (there is one report on smokeless tobacco) (Table 3.1). The land-mark first report was published in 1964 (U.S. Department of Health, Education, and Welfare [USDHEW] 1964), and the 50th-anniversary report, released in January 2014, comprehensively covered multiple aspects of cigarette smoking and health and lengthened the list of diseases caused by smoking and involuntary exposure to tobacco smoke (USDHHS 2014). Other Surgeon General’s reports that are particularly relevant to the present report include reports on the health consequences of smoking and involuntary exposure to tobacco smoke (USDHHS 2004, 2006), on the mechanisms by which smoking causes dis-ease (USDHHS 2010), and on the health consequences of smoking on youth and young adults (USDHHS 1994, 2012). The Surgeon General’s reports on smoking and health have provided powerful conclusions on the dangers of nicotine. The 1988 report, released by Surgeon General C. Everett Koop, was the first to characterize smoking as addictive, and it identified nicotine as “…the drug in tobacco that causes addiction” (Appendix 3.1)1 (USDHHS 1988, p. 9).
1All appendixes and appendix tables that are cross-referenced in this chapter are available only online at http://www.surgeongeneral.gov/
library/reports/
Table 3.1 Relevant conclusions from previous Surgeon General’s reports on smoking and health
Report Year Conclusions
The Health Consequences of Smoking: Nicotine Addiction (USDHHS 1988, p. 9)
1988 Major Conclusions
1. Cigarettes and other forms of tobacco are addicting.
2. Nicotine is the drug in tobacco that causes addiction.
3. The pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.
How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease (USDHHS 2010, p. 183)
2010 Chapter 4. Nicotine Addiction: Past and Present
1. Nicotine is the key chemical compound that causes and sustains the powerful addicting effects of commercial tobacco products.
2. The powerful addicting effects of commercial tobacco products are mediated by diverse actions of nicotine at multiple types of nicotinic receptors in the brain.
3. Evidence is suggestive that there may be psychosocial, biologic, and genetic determinants associated with different trajectories observed among population subgroups as they move from experimentation to heavy smoking.
4. Inherited genetic variation in genes such as CYP2A6 contributes to the differing patterns of smoking behavior and smoking cessation.
5. Evidence is consistent that individual differences in smoking histories and severity of withdrawal symptoms are related to successful recovery from nicotine addiction.
Preventing Tobacco Use Among Youth and Young Adults (USDHHS 2012, pp. 8, 460)
2012 Major Conclusions
1. Cigarette smoking by youth and young adults has immediate adverse health consequences, including addiction, and accelerates the development of chronic diseases across the full life course.
2. Prevention efforts must focus on both adolescents and young adults because among adults who become daily smokers, nearly all first use of cigarettes occurs by 18 years of age (88%), with 99% of first use by 26 years of age.
3. Advertising and promotional activities by tobacco companies have been shown to cause the onset and continuation of smoking among adolescents and young adults.
4. After years of steady progress, declines in the use of tobacco by youth and young adults have slowed for cigarette smoking and stalled for smokeless tobacco use.
5. Coordinated, multicomponent interventions that combine mass media campaigns, price increases including those that result from tax increases, school-based policies and programs, and statewide or community-wide changes in smokefree policies and norms are effective in reducing the initiation, prevalence, and intensity of smoking among youth and young adults.
Chapter 4. Social, Environmental, Cognitive, and Genetic Influences on the Use of Tobacco Among Youth
1. Given their developmental stage, adolescents and young adults are uniquely susceptible to social and environmental influences to use tobacco.
2. Socioeconomic factors and educational attainment influence the development of youth smoking behavior. The adolescents most likely to begin to use tobacco and progress to regular use are those who have lower academic achievement.
3. The evidence is sufficient to conclude that there is a causal relationship between peer group social influences and the initiation and maintenance of smoking behaviors during adolescence.
4. Affective processes play an important role in youth smoking behavior, with a strong association between youth smoking and negative affect.
5. The evidence is suggestive that tobacco use is a heritable trait, more so for regular use than for onset. The expression of genetic risk for smoking among young people may be
Report Year Conclusions The Health
Consequences of Smoking—50 Years of Progress (USDHHS 2014, p. 126)
2014 Chapter 5: Nicotine
1. The evidence is sufficient to infer that at high-enough doses nicotine has acute toxicity.
2. The evidence is sufficient to infer that nicotine activates multiple biological pathways through which smoking increases risk for disease.
3. The evidence is sufficient to infer that nicotine exposure during fetal development, a critical window for brain development, has lasting adverse consequences for brain development.
4. The evidence is sufficient to infer that nicotine adversely affects maternal and fetal health during pregnancy, contributing to multiple adverse outcomes such as preterm delivery and stillbirth.
5. The evidence is suggestive that nicotine exposure during adolescence, a critical window for brain development, may have lasting adverse consequences for brain development.
6. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to nicotine and risk for cancer.
Note: USDHHS = U.S. Department of Health and Human Services.
Table 3.1 Continued
Subsequent reports expanded on the conclusions in the 1988 report related to nicotine—reaffirming that nicotine causes addiction, describing nicotine’s effects on key brain receptors (USDHHS 2010), and emphasizing that youth are more sensitive to nicotine than adults and can become dependent to nicotine much faster than adults (USDHHS 2012). This is of particular concern in the context of e-cigarettes because blood nicotine levels in e-cigarette users have been reported as being compa-rable to or higher than levels in smokers of conventional cigarettes (Lopez et al. 2016; Spindle et al. 2015), and serum cotinine (a nicotine metabolite) levels have been reported as being equal to that found in conventional ciga-rette users (Etter 2016; Marsot and Simon 2016). Because of their sensitivity to nicotine and subsequent addiction, about 3 out of 14 young smokers end up smoking into adulthood, even if they intend to quit after a few years;
among youth who continue to smoke as adults, one-half will die prematurely from smoking (Peto et al. 1994;
CDC 1996; Hahn et al. 2002; Doll et al. 2004). Surgeon General’s reports have also emphasized the critical role of environmental determinants of tobacco use, including the causal roles of the tobacco industry’s advertising and promotional activities and of the peer social environment (USDHHS 2012).
The 2014 Surgeon General’s report included a chapter that addressed the numerous adverse conse-quences of nicotine other than addiction (USDHHS 2014).
The review documented the broad biological activity of nicotine, which can activate multiple biological path-ways, and the adverse effects of nicotine exposure during pregnancy on fetal development and during adolescence on brain development. Of concern with regard to cur-rent trends in e-cigarette use among youth and young adults, the evidence suggests that exposure to nicotine during this period of life may have lasting deleterious con-sequences for brain development, including detrimental effects on cognition (USDHHS 2014).
Finally, the aerosol from e-cigarettes may include other components that have been addressed in previous Surgeon General’s reports, such as tobacco-specific nitro-samines (TSNAs), acrolein, and formaldehyde (USDHEW 1979; USDHHS 2010). Aerosols generated with vapor-izers contain up to 31 compounds, including nicotine, nicotyrine, formaldehyde, acetaldehyde glycidol, acro-lein, acetol, and diacetyl (Sleiman et al. 2016). Glycidol is a probable carcinogen not previously identified in the vapor, and acrolein is a powerful irritant (Sleiman et al.
2016). Although these constituents have been identified in e-cigarette aerosol, current evidence is unclear on whether typical user dosages achieve levels as high as conventional cigarettes, or at harmful or potentially harmful levels.
More information will be available in the coming years as e-cigarette manufacturers begin reporting harmful or potential harmful constituents in compliance with the Tobacco Control Act.